Human cytomegalovirus (CMV), a ubiquitous species-specific herpesvirus and significant pathogen in immunocompromised individuals and neonates (Ho; Alford and Britt, 1993), is the best studied member of the betaherpesviruses (Morarski, 1993). Latent infection is a hallmark of all herpesviruses, and the neuronal site of latency of the alphaherpesviruses (such as herpes simplex virus-1) as well as the lymphoid site of latency of the gammaherpesviruses (such as Epstein-Barr virus) have been well-studied (Roizman and Sears, 1993; Liebowitz and Kieff, 1993). However, although latent infection by CMV is widespread and reactivation of latent virus after either immunosuppression or progressive immunodeficiency is the single most important contributor to emergence of CMV disease, the site(s) of viral latency remain poorly characterized (Mocarski, 1993).
Viral DNA has been detected in peripheral blood cells of healthy seropositive carriers (Bevan, et al., Taylor-Wiedeman, et al., 1991), and monocytes have been implicated as the most likely cell type harboring latent viral genomes (Taylor-Wiedeman, et al., 1991). Although the CMV genome persists in monocytes, virus does not reactivate during cultivation under conditions that stimulate growth and differentiation (Taylor-Wiedeman, et al., 1994). Thus, it has remained unclear whether monocytes, or other mononuclear cell types in peripheral blood, correspond to true sites of latency or simply reflect an occasional depository of viral DNA during sporadic reactivation or persistent infection (Ibanez, et al., Lathey and Spector, Schrier, et al.).
Two well-studied human CMV (HCMV) strains--Towne and AD169--have been sequenced (Stenberg, et al., 1984; Stenberg, et al., 1985; Boxhart, et al., 1985; Stenberg, et al., 1989; Chee, et al., 1990).